GI: Part 1 Flashcards
Large Intestine
Micro-organisms in the colon break down proteins left over from the small intestine. Amino acids are deaminated by the bacteria, leaving AMMONIA (Hepatic encepholapthy/altered mental status), which is then converted to UREA in the liver.
Liver
Carbohydrate metabolism
Glycogenesis, glycogenolysis, gluconeogenesis
Protein metabolism
Synthesis of nonessential amino acids, synthesis of plasma proteins, urea formation from NH3
Also synthesizes albumins, globulins, fibrinogens, and other proteins involved in clotting
Liver: Bilirubin
Bilirubin Metabolism:
Bilirubin is a pigment derived from the breakdown of red blood cells. Constantly being produced by the body.
It is insoluble in water so it is bound to albumin and transported to the liver. This is UNCONJUGATED bilirubin (Indirect Bilirubin)
Normal = 0-14 (p. 883, table 39.6)
In the liver, bilirubin combines with glucuronic acid and becomes soluble in water. This is CONJUGATED bilirubin (Direct Bilirubin) Normal = 0-5.1
Urea breath test
Urea breath test—rapid diagnostic test for Helicobacter Pylori. Based on the ability of H. Pylori to convert urea to ammonia. Patient inhales urea laced with radioisotopes. Exhaled breath analyzed. H.Pylori cause of peptic ulcers
Treat H pylori with 2 antibiotics, 1 PPI
Liver Biopsy
Used to obtain sample of hepatic tissue—analyzed for cancer, cirrhosis and fibrosis
Open Liver Biopsy—incision made and wedge of tissue removed.
Closed Liver Biopsy-percutaneous procedure. Patient lies in supine position with right arm above head. Needle inserted between 6th and 9th intercostal spaces on the right.
***Major complication—-BLEEDING. Patient is on bedrest for at least 6 hours post-procedure and lies on right side for first few hours to put pressure on the insertion point and minimize risk of hemorrhage.
Upper GI bleeding
Common causes:
Peptic ulcer disease
Primary factor is H. pylori, ingestion of ASA, NSAIDs, corticosteroids, smoking
Stress-related erosive syndrome
Decreased perfusion of stomach mucosa, related to physiological stress (decreased splanchnic perfusion)
Esophageal varices
Collateral circulation as a result of portal hypertension, rising pressure causes tortuous distended veins or varices
Peptic Ulcer Disease
Erosion of the GI mucosa resulting from the digestive action of HCL acid and Pepsin. ***H. Pylori present in more than 75% cases of gastric ulcers and 90% duodenal ulcers.
More common in women and those of low socioeconomic status.
***Increased incidence for smokers (nicotine promotes reflux of duodenal contents into the stomach), alcoholics, and those who take NSAIDs or ASA frequently.
Ulcers can perforate—require emergency treatment.
Upper GI Bleed
Mallory-Weiss tears
Laceration of the distal esophagus, gastroesophageal junction, and cardia of the stomach
Heavy alcohol use, binge drinking, forceful vomiting/retching, or violent coughing.
Dieulafoy’s lesions
Vascular malformations, usually in the proximal stomach
Upper GI Bleeding: Clinical Presentation
Orthostatic hypotension: increase in pulse > 20 bpm and drop in BP < 10 mmHg below baseline from sitting to standing Cool, clammy skin Hematemesis Hematochezia: blood in stool Melena: tarry black stool Coffee-ground emesis: blood with HCl upper GI bleed HIGH BUN: from hypovolemia Hypokalemia/Metabolic alkalosis
Lab Work for Upper GI Bleed
Decreased H& H
Mild leukocytosis & hyperglycemia (response to stress)
Increase BUN (large protein load from breakdown of Hgb)
Hypernatremia (result of emesis)
Hypokalemia (result of emesis)
Prolonged PT/PTT (liver dysfunction or use of anticoagulation?)
Thrombocytopenia (cirrhosis & portal HTN with splenomegaly)
Hypoxemia (decreased Hgb impairing O2 carrying capacity)
Classic Symptoms of GI Bleeding
Hematemesis
Indicates bleeding above the ligament of Trietz (suspensory muscle that connects duodenum to diaphragm)
Bright red indicates
active, profuse bleeding
“Coffee-ground” emesis is
RBCs broken down with HCL acid, causing it to turn brown
Classic Symptoms of GI Bleeding: Hematochezia
This is the passage of fresh blood through the anus, usually in or with stools.
Sometimes written as “BRBPR” Bright Red Blood Per Rectum
**Hematochezia is commonly associated with **lower GI bleeding, but may also occur from a brisk upper gastrointestinal bleed.
Classic Symptoms of GI Bleeding: Melena
Melena
Blood in the stools that turns them black (tarry) and foul smelling. The black color is caused by oxidation of the iron in hemoglobin during its passage through the ileum and colon
- **Indicates upper GI bleeding in 90% of cases
- **May take several days to clear stools
- **Stools will remain positive for occult blood for 1 to 2 weeks (detected by positive guaiac test)
Esophageal Varices:
Usually form as a result of liver cirrhosis. Complex of tortuous veins at the lower end of the esophagus. Swollen and engorged due to portal hypertension. Varices contain little elastic tissue and are quite fragile. May rupture as a result of coughing, sneezing, vomiting etc.
Management of UGI Bleeds
Two large-bore IVs or rapid central line insertion
Fluids- isotonic (normal saline)
Blood products (T&C for 4 units of PRBC stat). Calcium may drop, but it’s normal.
Fluids: LR or NS. May need CVP line or PA catheter to monitor effectiveness and avoid overresuscitation
T&C early!
If large amts of PRBCs transfused: hypocalcemia may result from citrate in stored blood that binds to calcium. Calcium administration may be required
OXYGEN!! To support tissue perfusion—prevents ischemia & dysrythmias
Foley insertion to monitor I&O
Vitamin K and/or FFP and platelets if coagulopathic
Vasoactives may be needed until fluid volume re-established
Upper GI Bleed Treatment
Gold Standard—patient needs EGD within 24 hours to identify bleeding lesion.
If bleeding ulcer identified, can use sclerosing agent such as Epinephrine. Also can place clips on the lesion to secure hemostasis.
Ulcers often re-bleed within 72 hours so continued treatment needed.
EVL—tx of choice for variceal bleeding (endoscopically placed rubber band)
ALTERNATIVE: Sclerotherapy (vasoconstricting agent causes necrosis and eventual sclerosis of bleeding vessel).
ANGIOGRAPHY if unsuccessful –intra-arterial vasopression or embolization w/ biodegradable sponges (temporary) OR steel coils, balloons, & silk threads (permanent)
Pharmacological Treatment for Upper GI Bleed
PPIs, Antacids, Cytoprotective agents (Sucralfate), H2 Blockers
Antibiotics for H. Pylori (Flagyl & Tetracycline)
Vasopressin (Pitressin) drip—splanchnic vasoconstriction. Reduces portal blood flow. Can cause systemic
vasoconstriction (risk of myocardial ischemia, chest pain)
Octreotide (Sandostatin) drip-decreases splanchnic blood flow and HCL acid production. Commonly used. Given as a drip for about 3 days.
Vasopressin, Somatostatin, & Octreotide (Sandostatin) all decrease portal pressure by constricting the splanchic arteries.
With Vasopressin & Sandostatin—concurrent use of NTG recommended b/c coronary blood flow reduced and vasopressin increase BP causing increased oxygen demand (can lead to cardiac dysrhythmias)
Ruptured Esophageal Varices
Medical emergency!
Patient can exsanguinate and/or lose airway quickly
May need intubation and critical interventions rapidly
Can place esophageal tamponade device
Sengstaken-Blakemore tube (3 ports)
Minnesota tube (4 ports)
If chest pain: gastric balloon deflated and shifted to esophagus??
If gastric balloon ruptures, esophageal balloon can migrate upwards and occlude airway!!
Sengstaken-Blakemore Tube
Gastric = anchor Esophageal = tamponade If gastric balloon ruptures, esophageal balloon can migrate upwards and occlude airway Elevate HOB (high Fowler’s) Scissors at bedside Gentle tension to tube
Lower GI Bleeding
Most common causes:
***Malignant tumors
***Ischemic colitis and infectious colitis from C. Diff
Diverticulosis
Hemorrhoids
Massive upper GI hemorrhage
Hepatitis
Can also be caused by alcohol, drugs (e.g.Tylenol), chemicals and autoimmune liver disease
Viral hepatitis-major public health concern in the U.S.
Acute hepatitis lasts less than 6 months
Resolves completely or progresses to chronic hepatitis, then cirrhosis, then liver failure
Noninfectious hepatitis
Excessive alcohol use (Laennec’s cirrhosis)
Autoimmune disorders
Biliary obstruction
Medications (Tylenol, antilipemic -statins)
Right-sided heart failure
Hepatitis A
Fecal / oral route
Polluted water / food especially raw or undercooked shellfish
Sexual transmission
15-45 days incubation –pt asymptomatic but HIGHLY contagious
Symptoms are mild (flu-like) or sometimes non-existent. Older pts more at risk for more sever symptoms.
Most commonly seek medical attention due to jaundice & hepatomegaly. By this time, virus no longer shedding and not contagious.
Usually complete recovery. NO chronic type or leading to cirrhosis
Hepatitis B
Sexual transmission common but usually needs a break in the mucosa
Causes both acute & chronic hepatitis
Acute phase-fever, rash, arthralgia
Can progress to cirrhosis with very high mortality rate
Vaccinate!!!
Treat with anti-virals—Interferon, Lamivudine etc
Hepatitis C
Hep C virus (HCV) leading cause of liver cirrhosis requiring transplant in the U.S.
Usually blood-borne. Frequently seen with IVDA, possibly sexual contact, also with body piercing etc.
Incubation 15-160 days
Goal of treatment is to eradicate viral load—treat with Interferon, Ribavirin, other anti-virals
No vaccine available
Hepatic Cirrhosis
Extensive degeneration and destruction of the liver parenchymal cells.
Overgrowth of new fibrous tissue distorts the liver’s normal structure, with the result that blood flow is impeded.
Disorganized regeneration, poor cellular nutrition and tissue hypoxia leads to the formation of scar tissue and impaired function.
Nonalcoholic fatty liver disease
The accumulation of fat in the cells leads to inflammation and scarring. This is referred to as Non Alcoholic Steatohepatitis or NASH.
Development of NAFLD is directly related to body weight and is a major complication of obesity. There is also a correlation between NAFLD and the use of diltiazem and amiodarone.
Assessment for NFLD
Jaundice, hepatomegaly, splenomegaly
Muscle wasting, ascites, peripheral edema
Vitamin deficiencies, bruising, telangiectasis, spider nevi (portal hypertension)
Abdominal wall vein dilation (caput medusae)
Bruit over the liver
Clay-colored stools (think about bilirubin metabolism)
Palmar erythema
Fetor hepaticus: Ammonia smelling breath
Hepatic encephalopathy
Tests for NFLD
Tests for evaluating hepatocellular injury
AST, ALT
***Tests for evaluating liver synthetic function
(Low) Albumin, (Low) total protein, and (High) PT
Tests for evaluating cholestasis (excretory function)
Serum bilirubin
Alkaline phosphatase and GGT
Complications of liver failure
Coagulopathies—PT often very high—requires transfusion of FFP
Ascites (altered protein metabolism leads to impaired albumin synthesis). Can do abdominal paracentesis, LeVeen (venous-peritoneal) shunt. Give 25% Albumin.
***Encephalopathy—ammonia, urea. Hyperosmotic laxative—LACTULOSE! Normal ammonia level (NH3) 15-49 mcq/dl (Varies by institution)
Hypoglycemia—may need D10, D20 or D50 drip
***Hepatorenal syndrome common. Impaired circulating volume and albumin synthesis lead to low-pressure issues in the kidney.
LeVeen Shunt
Shunt with one end in the peritoneum, the other tunneled into a central vein. Allows for ascites to be reabsorbed into the circulation
Complications of liver failure
Encephalopathy—ammonia, urea. Hyperosmotic laxative—LACTULOSE! Normal ammonia level (NH3) 15-49 mcq/dl (Varies by institution)
***Don’t hold the lactulose because the patient develops diarrhea!!! They will end up in a coma.
Lactulose facilitates BMs to help clear nitrogenous products and decreases the bowel Ph which prevents absorption of ammonia.
Neomycin & metronidazole: clears gut of bacteria that promote nitrogenous production.
Protein intake limited to 20-40 g/day
Hemorrhage in liver failure
Splenomegaly results from backup of blood from portal vein leading to thrombocytopenia, leukopenia and anemia.
Failing liver is unable to produce prothrombin and other essential clotting factors.
Bruising, petechaie, bleeding
Portal Hypertension
Increase in portal venous pressure with vasoconstriction
Blood cannot enter the liver so it shunts away down other channels
Bleeding of esophageal varices major complication
Esophogeal Varices Treatment again lol
Avoid irritants, coughing
Medications: Vasopressin (Pitressin), Aquamephyton (Vit K), Beta Blockers
Endoscopy
Tamponade (Blakemore tube)
TIPS procedure
Surgical Management for Esophageal Varicies
Transjugular Intrahepatic Portosystemic Shunt (TIPS)
Procedure of choice for varices
Involves placement of a stent between portal and systemic circulation to redirect blood flow and depressurize the portal veins
TIPS- transjugular intrahepatic portosystem shunt for ascites & bleeds. Stent in portal vein that diverts blood flow and decreases portal HTN. Portal vein to hepatic vein which empties blood into the IVC
Liver Transplantation
Liver transplantation is the only definitive, proven treatment for acute hepatic failure
Abbreviated as OLTx—Orthotopic Liver Transplant.
Orthotopic—take the old one out, put the new one in. Not piggybacked.
Sometimes donated liver is split and given to two recipients (works better in pediatric pts)
Most common reasons for Liver Transplantation
Hep C
Laennec’s cirrhosis
NASH
Fulminant hepatic failure—when liver ceases to function abruptly—often due to drug overdoses (e.g Tylenol, Ecstasy)
